Journal of Experimental Medicine, Vol 167, 89-108, Copyright © 1988 by Rockefeller University Press

ARTICLES

A nonimmunosuppressive helper virus allows high efficiency induction of B cell lymphomas by reticuloendotheliosis virus strain T

CF Barth and EH Humphries
Department of Microbiology, University of Texas Health Science Center, Dallas 75235.

We have documented the effect of two nondefective helper viruses, reticuloendotheliosis virus A (REV-A) and chick syncytial virus (CSV) infection on bursal tissue. REV-A infection results in bursal atrophy, destroying both its structural and functional integrity. In contrast, the bursae in CSV-infected chicks, while reduced slightly in size, appear both structurally and functionally normal. REV-A-induced bursal atrophy is not a result of viral replication in the B-lymphocyte as (a) both viruses are capable of inducing, with equal efficiency, the formation of preneoplastic lesions containing proliferating B lymphocytes and (b) it appears that equivalent amounts of viral antigen are expressed in the bursae of chicks infected with either virus. We have examined the phenotype of tumors induced by the replication- defective virus REV-T when replicated by the two different helper viruses, REV-A and CSV. In REV-T(REV-A)-infected chicks, the majority of tumors that develop are negative for IgM expression. In contrast, the majority of tumors induced by REV-T(CSV) infection are IgM+. This finding is confirmed by recovery of IgM- cell lines from REV-T(REV-A)- infected chicks and IgM+ cell lines from REV-T(CSV)-infected chicks. In addition, repopulation studies show that bursal-derived cells that are IgM+ serve as target cells for REV-T(CSV)-induced lymphomas. This study demonstrates, therefore, that REV-T can induce IgM+, B cell lymphomas with high efficiency. We conclude that infections by the helper viruses, REV-A and CSV, differ dramatically in their effects on the composition of the population of cells that serve as targets for REV-T- induced neoplasia.
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This article has been cited by other articles:

• Carlson, L M, McCormack, W T, Postema, C E, Humphries, E H, Thompson, C B (1990). Templated insertions in the rearranged chicken IgL V gene segment arise by intrachromosomal gene conversion.. Genes Dev. 4: 536-547 [Abstract]  
• McCormack, W T, Tjoelker, L W, Barth, C F, Carlson, L M, Petryniak, B, Humphries, E H, Thompson, C B (1989). Selection for B cells with productive IgL gene rearrangements occurs in the bursa of Fabricius during chicken embryonic development.. Genes Dev. 3: 838-847 [Abstract]  

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